[Interaction among abnormal fatty acid oxidation, endothelial function disorder, and oxidative stress in the onset of severe preeclampsia].
OBJECTIVE
To investigate the association of abnormal fatty acid oxidation (FAO), endothelial function activation, and oxidative stress in pathogenesis of severe preeclampsia ( S-PE).


METHODS
Placenta tissues were obtained from 70 S-PE patients with onset in different gestational weeks with or without liver damage. The protein expression of long chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD), tumor necrosis factor (TNF)-alpha, vascular cell adhesion molecule (VCAM)-1, and peroxisome proliferator activated receptor (PPAR) gamma were analyzed using immunohistochemistry. 54 samples from normal pregnancy in first, second and third trimester were collected as controls.


RESULTS
Protein expression of LCHAD, TNF-alpha, VCAM-1, and PPARgamma could be seen in both placenta of normal pregnancy and S-PE. The protein expression on level of LCHAD of the cases of S-PE that came down of the disease before 32 gestational weeks, especially of the cases complicated with liver damage, was significantly lower than that of the controls (P < 0.05). However, no differences in the LCHAD protein expression were found between the S-PE patients with the onset after and 32 gestational weeks and the controls. The TNF-alpha protein expression levels of the S-PE patients with different onset weeks were all significantly higher than those of the controls (all P < 0.05). The VCAM-1 protein expression levels of the S-PE patients with the onset after 34 gestational weeks was significantly higher than that of the controls (P < 0.05). There was no significant difference in the PPARgamma protein expression between the S-PE patients and the controls. The placental LCHAD protein expression of the S-PE patients with the onset before 32 gestational weeks, especially of the cases with liver function damage, was dramatically decreased in comparison with the controls, and the placental TNF-alpha protein expression was dramatically increased, however, there was no linear correlation between LCHAD and TNF-alpha expression. There was no significant difference in expression of PPARgamma and VCAM-1 between the S-PE patients and the controls. There was no linear correlation among the expression levels of LCHAD, TNF-alpha, VCAM-1, and PPARgamma between the S-PE patients with the onset before and after 32 gestation weeks.


CONCLUSIONS
Abnormal FAO may be one of the factors related to some cases of PE with the onset before 32 gestational-weeks, especially those with liver damage. The correlation among LCHAD, TNF-alpha, VCAM-1, and PPARgamma are complicated.
Wang
Jia-lue
JL
Department of Obstetric and Gynecology, Peking University Third Hospital, Beijing 100083, China.
Yang
Zi
Z
Wang
Rong
R
Zhu
Jin-ming
JM
D000328:Adult; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000503:physiopathology; D005227:Fatty Acids / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D050356:Lipid Metabolism; D018384:Oxidative Stress; D047495:PPAR gamma / Q000378:metabolism; D010920:Placenta / Q000378:metabolism; D011225:Pre-Eclampsia / Q000378:metabolism* / Q000503:physiopathology; D011247:Pregnancy; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D055815:Young Adult
D005227:Fatty Acids; D047495:PPAR gamma; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1